Currently, in the medical field, as it pertains to pulmonary and/or circulatory system diseases in animals, stents (such as in coronary arteries) and grafts (such as used in the Aorta) provide an important treatment modality used both to treat narrowing or occlusion of the arterial lumen (e.g., in coronary artery disease or renal artery stenosis) as well as for widening of the lumen because of a disease in the vessel wall (e.g., an aortic aneurysm). Vascular stents are usually made of metal and vascular grafts are commonly made of Dacron.
Narrowing of the lumen of a stent or graft may follow implantation. This may be due to proliferation of tissue surrounding the stent or graft (restenosis). Narrowing of the lumen of a stent or graft may also be due to the formation of a blood clot on the surface of a stent or graft facing the vessel lumen (e.g. in-stent thrombosis). Patients with a coronary artery stent are usually prescribed medications to prevent blood clot formation on the stent. Narrowing of the lumen of a stent or graft may further be caused by an embolus from another part of the body that cannot pass through a stent or graft, said embolus be composed of a blood clot, microorganisms, or fat.
Noninvasive measurement of blood flow across an intravascular device is inaccurate and requires special equipment and expertise which are not readily available. Occlusion of a coronary artery by in-stent thrombosis may result in sudden cardiac death from a myocardial infarction (heart attack) or a fatal arrhythmia. Occlusion of a stent elsewhere can cause ischemia and infarction of tissues supplied by the vessel in which the stent had been implanted.
Moreover, the gold standard methods for cardiac output measurement are invasive, complicated and risky.
It is the case that non-invasive assessment using external ultrasound-Doppler devices is less accurate.
However, cardiac output measurement is key to diagnosing and treating both acute and chronic conditions. For example, it is clinically important and useful to know whether a patient presenting with shortness of breath suffers from a primary respiratory pulmonary disease or from a heart problem.
Cardiac output may change in the presence of volume overload, pressure overload and ischemia. Changes in cardiac output may precede the clinical manifestations of diseases. For example, reduced cardiac output may precede the development of pulmonary edema. Early cardiac ischemia may cause impaired relaxation of the ventricular wall, leading to decreased cardiac output even before acute ischemia (e.g. myocardial infarction) is present. A cardiac arrhythmia may be asymptomatic but lead to decreased cardiac output. For example, atrial fibrillation, a common arrhythmia that may go unnoticed by a patient reduces cardiac output by eliminating the “atrial kick” that actively pumps blood into the ventricle.
Furthermore, failure of a prosthetic valve may be the result of prolonged wear and tear but may also indicate a dangerous but potentially curable condition like stuck valve (the formation of a blood clot on the valve compromising leaf movement) or infection or inflammation causing vegetation formation on the valve.
Changes in the flow across a prosthetic heart valve may also be the result of leakage around the valve (paravalvular leak). These conditions may be insidious and thus diagnosis may be delayed, or they could be abrupt, resulting in a medical emergency.
Assessment of a valve function is most commonly done using echocardiography, which requires special equipment and professional operation, and thus is not readily available on demand.
Artificial hearts are used when a patient's native heart has failed either temporarily (e.g. during the course of myocarditis or acute ischemia) or permanently (e.g. due to dilated cardiomyopathy). Various designs have been developed, propelling blood in addition to or instead of one or more compartments of the heart. These devices have high energy consumption and are prone to blood clot formation or infection that may reduce their function.